Magnetotactic bacteria can orient and migrate along ambient geomagnetic field lines because of their intracellular magnetic particles ( referred as magnetosomes) , which comprise nanometer-sized, membrane-bound crystals of the magnetic iron minerals. Magnetosome formation is a mineralization process with very strict biological controls over the accumulation, transportation and nucleation in the cell. This paper describes the current progresses of magnetosome formation and the function of proteins involved in this biomineralization process.

Aim To investigate whether necroptosis mediates chemical hypoxia-induced HT22 mouse hippocampal cell injury and inflammation.Methods HT22 hippocampal cells were exposed to cobalt chloride (CoCl2) to establish a model of the chemical hypoxia-induced injury and inflammation.The expression level of RIP3 (an index of necroptosis) was determined by Western blot.Cell counter kit-8 (CCK-8) assay was used to test the cell viability.Lactate dehydrogenase (LDH) activity in the culture medium was measured with commercial kits.Mitochondrial membrane potential (MMP) was examined by rhodamine123 staining followed by photofluorography.The intracellular level of reactive oxygen species (ROS) was detected by 2', 7'-dichlorfluorescein-diacetate (DCFH-DA) staining followed by photofluorography.The secretion levels of interleukin-1β (IL-1β) and tumor necrosis factor-a (TNF-α) were measured by ELISA.Results Treatment of HT22 hippocampal cells with 600 μmol·L-1 CoCl2 for 36 h markedly induced cytotoxicity, leading to a decrease in cell viability to (52.0±2.65) % , indicating that chemical hypoxia-induced cellular injury model was successfully set up.Besides, CoCl2 induced considerable injuries and inflammation, evidenced by increases in LDH activity, ROS production, MMP loss, as well as the secretion levels of IL-1β and TNF-α.Co-treatment of the cells with 40~100 μmol·L-1 Nec-1 (a specific inhibitor of necroptosis) and CoCl2 markedly attenuated the decrease in viability induced by CoCl2, reaching the best anti-cytotoxicity inhibitory effect at 80 μmol·L-1.Meanwhile, the co-treatment with 80 μmol·L-1 Nec-1 blocked the above injuries and inflammatory response induced by CoCl2.In addition, treatment of HT22 hippocampal cells for 6~48 h up-regulated the expression of RIP3, and Nec-1 alleviated the up-regulation of RIP3 expression level induced by CoCl2.Conclusion Necroptosis mediates chemical hypoxia-induced HT22 hippocampal cell injury and inflammation.

Objective To evaluate the effects of bone morphogenetic protein 2(BMP-2)gene modified tissue engineering bone combined with vascular bundle implantation in repairing segmental bone defect.Methods The isolated rabbit hone marrow stromal cells(MSCs),after being transfected by adenovirus carrying BMP-2 gene(Ad-BMP-2),were seeded on bovine cancellous bone scaffolds(BCB) to construct gone modified tissue engineering hone.The rabbit models with radial defects(2.0 cm long) were made and repaired with four methods including gene modified tissue engineering bone with vascular bundle implantation(Group A),gene modified tissue engineering bone(Group B),nongene modified tissue engineering bone with vascular bundle implantation(Group C),and only BCB scaffolds(Group D).After 4,8,and 12 weeks of operation,X-ray,histological examination,biomechanics analysis and capillary vessel ink infusion were conducted to observe angiopoiesis and osteogenesis.Results Group A gained better effect in the volume and activity of new bones than other groups,with vascular bundle sending out new branches into the transplanted bones and productive regeneration of capillary vessel.The defect in Group A was repaired satisfactorily.Group B showed better effect in speed and quality of bone formation than Group C under induction of BMP-2 gent.Mainly fibrous tissues but not new bones were observed in Group D.Conclusion BMP-2 gene therapy with vascular bundle implantation has very strong osteoinduction ability and quite good vascularization effect and is of great value to the treatment of bone nonunion and bone defects.

Objective To analyze the relationships between the drinking water fluoride and bone mineral density (BMD), and serum osteocalcin (BGP) and to explore the BMD and serum BGP as significant early screening biomarkers for fluorosis especially for early bone damage in endemic fluorosis areas. Methods Wamiao (severe endemic fluorosis area, as fluoride exposed group) and Xinhuai (non endemic fluorosis area, as control group) Village were selected in 2006. One hundred and fouty-six objects were chosen from 2 villages (103 in Wamiao, 43 in Xinhuai). The sex, age, body height, body weight, drinking water fluoride in each object's household well, BMD, and serum BGP were investigated, and the dose-response relationships were analyzed between the drinking water fluoride and BMD, and serum BGP. CurveExpert 1.3 Software was used to fit the dose-response relationships between the rate of abnormal BMD, the rate of abnormal serum BGP, and the drinking water fluoride. Results The levels of drinking water fluoride in males' and females' families in fluoride exposed group were [(2.38±0.68), (2.62±0.91 )mg/L] significant higher than that in control group [(0.35±0.08), (0.36±0.07)mg/L], the difference being statistically significant(t values were 14.27 and 11.08,and P<0.01, respectively). BMD in males in fluoride exposed group [(0.78±0.07)g/cm2] was significant lower than that in control group[(0.83±0.08)g/cm2], the difference being statistically significant (t=2.37,P<0.05). Serum BGP in males and females in fluoride exposed group [(4.17±0.67), (4.11±0.57) μg/L] were significant higher than that in control group [(1.48±0.40), (1.44±0.39)μg/L], the difference being statistically significant (t values were 17.64 and 19.40, and P<0.01, respectively]. BMD in the group with drinking water fluoride≥2.92 mg/L[(0.66±0.15 )g/cm2] was significant lower than that in the group with drinking water fluoride<0.42 mg/L [(0.76±0.12)g/cm2], the difference being statistically significant (P<0.01). The levels of serum BGP in the groups with the drinking water 0.42-,2.05-, ≥.92 mg/L[(3.83±1.07), (4.22±0.72), (3.99±0.63) μg/L] were significant higher than that in the group with the drinking water<0.42 mg/L [(1.44±0.37) μg/L], the difference being statistically significant (P<0.01). The equation for the dose-response relationship between the drinking water fluoride and the rate of abnormal BMD was y=(0.284-0.058x)-1.260, r=0.999 94; and y=100.05/(1+78.62e-4.5x), r=0.999 99 for the drinking water fluoride and the rate of abnormal serum BGP. Conclusions There were significant dose-response relationships between drinking water fluoride and BMD and serum BGP. It indicated that BMD and BGP might be considered as early screening biomarkers for endemic fluorosis, especially for the bone damage.

Objective To study the changes of somatostatin(SOM) in plasma and cerebrospinal fluid (CSF) of children with convulsive diseases.Methods Sixty-seven children with convulsive diseases were studied as following:obtaining the samples of plasma in the 1st and 7th day after being in hospital,and the samples of CSF in the 1st after being in hospital.We investigated the changes of SOM in plasma and CSF with radioimmunoassay(RIA).Results 1.Convulsive group:the concentration of SOM in plasma in the 7th day(29.47?9.40 ng/L) was significant lower than that in the 1st day(39.23?11.00 ng/L)(t=21.530 P0.05).The concentration of SOM in plasma in the 1st day in control group was(19.58?6.04) ng/L.There were significant differences in convulsive group and encephalitis group without convulsion, control group(t= 6.847,7.921 P

Objective To discuss the clinical effect of intertrochanteric fracture treated with InterTan intramedullary nail. Methods Between Jan 2011 and June 2006 , 100 consecutive patients with intertrochanteric fracture were treated with a new nail (InterTan). We recorded the operation time, blood loss, blood transfusion volume and the modified Harris hip score was used to evaluate outcomes. Results All cases were received follow-up of 6 to 15 months. All cases got bone healing and did not appear various complications. The modified Harris hip score were (75.1 ± 13.4) points. Conclusion The InterTan device appears to be a reliable implant for treatment of intertrochanteric femoral fractures.

To improve 3-ketosteroid-△1-dehydrogenase(KSDH) activity and the transformation level for androst-4-ene-3,17-dione, 3-ketosteroid-△1-dehydrogenase gene(ksdD) from Arthrobacter simplex was cloned into plasmid pWB980 and expressed in B. subtilis WB600 under the control of promoter P43. The molecular weight of expressed enzyme was about 55kDa by SDS-PAGE analysis. The activitities assayed by spectrophotometrical method of intracellular and extracellular soluble enzyme were 110?0.5mU and 15?0.6mU per milligram of protein respectively. The transformation rate of androst-4-ene-3,17-dione by the B. subtilis recombinant cells was 45.3%. Compared with Arthrobacter simplex, the enzyme activity of KSDH expressed in B. subtilis was improved about 30 fold, and the transformation level of androst-4-ene-3,17-dione by the B. subtilis recombinant cells was improved about 10 fold. The recombinant B. subtilis cells used in biotransformation of steroids provided a new way for steroid medicines production.

Abdominal Pain/etiology* ; Acute Disease ; Appendicitis/diagnosis* ; Diabetes Mellitus ; Diabetic Ketoacidosis/diagnosis* ; Diagnostic Errors/adverse effects* ; Humans ; Insulin

Hepatitis B virus (HBV) represents a significant global public health challenge. Despite the availability of several approved drugs for hepatitis B treatment, the persistence of covalently closed circular DNA (cccDNA) renders HBV eradication elusive, thereby leading to disease relapse after drug withdrawal. This paper reviews the regulatory mechanisms of cccDNA formation, transcription and replication, and summarizes the research progress of related small molecule regulators from the perspective of medicinal chemistry.

Hepatitis B virus infection is a serious threat to human life and health. The approved anti-HBV drugs including interferons and nucleos(t)ide analogues have serious adverse effect, rebound phenomena after drug withdrawal, and drug resistance. And the cccDNA cannot be completely eliminated by both of them, which is the reason why a complete cure for hepatitis B cannot be achieved. Therefore, developing anti-HBV drugs directly targeting protein or nucleic acid of HBV remains a current public health priority. Based on the analysis of representative literature from the last decade, this article reviews recent developments in small molecule inhibitors directly targeting HBV from a medicinal chemistry perspective.